Key result
The renin-angiotensin system plays a critical role in the initiation and progression of atherosclerosis through mechanisms involving reactive oxygen species and inflammation.
The local renin-angiotensin system in both the vasculature and bone marrow plays a critical role in the progression and destabilization of atherosclerosis, highlighting AT1R blockade as a key therapeutic strategy.
Supports RAS inhibition research in atherosclerosis; leaves open prospective trials before clinical adoption.
The renin-angiotensin system (RAS) has been demonstrated to play a critical role in the initiation and progression of atherosclerosis, thereby contributing to development of cardiovascular diseases. Angiotensin II (Ang II), a major substrate in RAS, stimulates atherosclerosis through various deleterious effects such as endothelial dysfunction, cellular proliferation and inflammation. Recently, local RAS in vasculature is reported to play an important role. Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Investigation of the role of ROS and inflammation induced by RAS may provide a clue to understanding the pathophysiology of atherosclerotic diseases, and may lead to a new therapeutic strategy.
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Sata et al. (2010) conducted a review in Atherosclerosis. Renin-angiotensin system (RAS) blockade was evaluated. The renin-angiotensin system plays a critical role in the initiation and progression of atherosclerosis through mechanisms involving reactive oxygen species and inflammation.
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